Exam 4 Review New Flashcards
Alveolar PO2 alveolar
104 mmHg
Alveolar PCO2 alveolar
40 mmHg
Inspired Air PO2
159 mmHg
Inspired Air CO2
0.3 mmhg
Expired Air PO2
127 mmHg
Expired Air PCO2
28 mmHg
Tissues PO2
40 mmHg
Tissue PCO2
46 mmHg
From Heart and systemic Circulation PO2
40 mmHg
From Heart and systemic Circulation CO2
46 mmHg
To Heart and systemic Circulation PO2
100 mmHg
To Heart and systemic Circulation CO2
40 mmHg
Calculating VE = minute ventilation (volume per minute) Example:
VE = vT x f = 500 x 10 = 5000 ml/min.
VE=
tidal volume (volume per breath) x frequency or RR (Respiratory Rate)
VA =Alveolar ventilation
VA= (VT – vDS) x RR
VDS = and Example
physiologic dead space ~ 1ml per pound ideal body wgt 150 lbs patient VA = (VT–vDS ) x RR = (500 – 150) x 10 = 3500 ml/min.
Tests of Ventilatory Capacity: • DLCO –
tests diffusing capacity of the alveolar-capillary membrane
FEV
(Forced Expiratory Volume)
FVC (Forced Vital Capacity) –
Assesses progression of lung disease – Assesses efficacy of bronchodilators
FEF (Forced Expiratory Flow) –
Assesses average flow rate
Single-breath Nitrogen Test –
Assess dead space & presence of small airway disease
FRC (functional residual capacity) is the
volume remaining in the lungs at the end of a normal tidal expiration
Forced Expiratory Volume – • Written as FEV1
The vol. of gas exhaled in 1 sec. by a forced expiration from full inspiration.
Normal ratio of FEV1 to FVC =
80% (decreases w/age)
FEF25-75%
• The middle half (by volume) of total expiration
Single-breath Nitrogen Test • Can be used to calculate
deadspace and assess for early lung disease in the small airways.
Explain single breath nitrogen Test
• Pt. takes a vital capacity breath of 100% O2, then exhales slowly through mouthpiece w/ N2 sensor.
Single-breath Nitrogen Test: Phase 1:
Pure O2 exhaled, [N]=0
Single-breath Nitrogen Test Phase 2
Phase 2: [N]↑ as deadspace washed out by alveloar air.
Single-breath Nitrogen Test Phase 3:
alveolar plateau – nearly flat in normal patients; steeper slope in lung disease.
Single-breath Nitrogen Test Phase 4:
↑ as least ventilated areas of lungs empty (more N b/c little or none of the 100% O2 reached these areas in the previous inspiration, Little dilution)
Single-breath Nitrogen Test
Slopes in Phase 3 and 4 are steeper in uneven ventilation 2o to disease (and age).
3 possible mechanisms of uneven ventilation:
Partial obstruction “parallel” ex. asthma
Dilation (↓diffusion) “series” ex. ex. emphysema
Complete obstruction “collateral” ex. COPD
Emphysema
• Destruction of alveolar walls and lung elastin by neutrophil elastase, with dilation of airways distal to terminal bronchioles.
Partial capillary bed destruction =
V/Q mismatch =dead space & pulmonary HTN
↓ surface area =
↓diffusing capacity, ↓ gas exchange
Pink puffers ” • Non productive cough
PO2 normal ∴“pink” no cyanosis
PInk puffers lung
• Have decreased lung elastic recoil
Pink puffers: What causes air trapping?
Air trapping is caused by loss of normal dynamic compression ∴ pursed lips as patients learn that prolonging expiration phase keeps the airways open slightly longer
Pink puffers: Tachypnea gives appears of a
“puffing”
Pink puffers Complications of emphysema: –
Pneumothorax 2o to ruptured bullae – Weight loss 2o to ↑ work of breathing
Emphysema Signs/Symptoms: Lung Decreased values
• FEV1 , FVC, FEV/FVC%, FEF25-75% all decreased
Emphysema Signs/Symptoms:
• Barrel chest , dyspnea, weight loss, ↓breath sounds
CXR –> with EMPHYSEMA there is
CXR: Hyperinflation Hyperlucency Low set flat diaphragm Vertical heart
Lateral CXR What do you see ?
Normal vs. Emphysema • Increased retrosternal clear space & kyphosis
Chronic Bronchitis
• Too much mucus 2o to↑ irritants – Smoking/Pollution/coal/asbestos/allergens/genetic – Smoking also destroys cilia, compromising mucociliary escalator
Chronic Bronchitis there is
↑ airway resistance
• Air trapping
↑TLC secondary to mucus plugs
In chronic bronchitis there is ↑ barrier thickening =
↓ gas exchange
Chronic Bronchitis and Smooth muscle bronchospasm
Smooth muscle bronchospasm 2o to inflammation
Diagnosis of Bronchitis
• Dx: 3 mo. x 2 yrs.
In Chronic bronchitis, Bronchial lumen narrowed 2o to: –
Excessive mucus (infection can occur behind mucus plugs) – Thickened wall • smooth muscle spasm • Hypertrophy & hyperplasia of mucus glands
Chronic Bronchitis and– Reid index
Reid index = ratio of mucus glands to thickness of wall • Normal < 40% in CB >40%
“Blue Bloater” (Type B COPD) • Frequently obese
• Cyanosis “blue” discoloration • Hypoxia/Hypercapnia/Dyspnea • JVD
Blue Bloater cough
• Chronic productive cough • Purulent sputum
Complications of CB:
– Polycythemia 2o to hypoxemia – Plumonary HTN 2o to hypoxic vasoconstriction – Cor pulmonale 2o to chronic pulm. HTN
Chronic Bronchitis
• FEV1 , FVC, FEV/FVC%, FEF25-75% all decreased
Sign/Symptoms Chronic Bronchitis
• Cyanosis, hypoxia, dyspnea • Rales & ronchi • Chronic productive cough 3mo. x 2yrs.
Chronic Bronchitis • Other tests:
– PFT – HRCT – Sputum exam
Pulmonary Fibrosis there is ______Resulting in _______compliance
• Thickening of alveolar wall = ↓ compliance
Exact cause of Pulmonary Fibrosis
Unknown
Pulmonary Fibrosis is due to repeated ________causing______
• Repeated exposure to irritant causes abnormal repair response with scarring
Can cause pulmonary Fibrosis (SEGIV)
– Smoking – Environmental dust exposure – GERD – Industrial oxidants – Viral infections
Pulmonary Fibrosis, alveolar cells • • Uncontrolled, dysregulated deposition of extracellular matrix = thickened, stiffened fibrosis
• Alveolar cells injured
Release profibrotic & inflammatory mediators:– TNF-α
– recruit inflammatory cells
Release profibrotic & inflammatory mediators– TGF-β
stim. migration & proliferation of . migration & proliferation of fibroblasts
Release profibrotic & inflammatory mediators–
Growth factors stim. migration of myofibroblasts
Mediators Organize into
clusters called fibroblastic foci
Uncontrolled, dysregulated
deposition of extracellular matrix = thickened, stiffened fibrosis
Pulmonary Fibrosis: airway
• Excessive radial traction increases airway caliber
Pulmonary Fibrosis Clinical Manifestations
Clinical Manifestations • Affects adults 50s-60s • Dyspnea on exertion • Tachypnea with small TVs • Nonproductive cough
Lung Volumes changes in Pulmonary FIbrosis
• FVC ↓↓↓ • FEV1 normal to low • FEV/FVC%↑ • TLC & FRC ↓↓↓
Pulmonary Fibrosis • CXR: RHL
Reticulonodular pattern, especially at the bases Honeycomb appearance in late ds. Lungs typically small, w/ raised diaphragms
Pneumothorax
Penetrating chest wound or ruptured bleb allows air in P.C. = passive recoil of lung away from chest wall
Spontaneous Pneumothorax: common
Most common form
Spontaneous Pneumothorax: small bleb
Rupture of small bleb on surface near apex
Spontaneous pneumothorax typically occurs in
Typically occurs in young males
Spontaneous pneumothorax related to
Related to high mechanical stresses in upper zone of upright lung – Presents with sudden pain & dyspnea
Tension Pneumothorax
• Occurs when the defect acts as a one-way valve • Air enters pleural space on inspiration but cannot be expelled on expiration
What happens in spontaneous pneumothorax
Air entrained with each breath –Increasing pressure causes compression of contralateral lung and Decrease venous return
Tension Pneumothorax occurs
↓ ↓ venous return – Surgical Emergency
Pulmonary Edema: Pathogenesis
• Increased Capillary Permeability • High Permeability Edema (High K) • High Protein & RBCs
Pulmonary Edema Caused by
– Inhalation injury – toxins, oxygen poisoning – Circulating factors – inflammatory mediators, endotoxins – ARDS
Pulmonary Edema: Pathogenesis Intersitital Hydrostatic pressure
• Decreased Interstitial Hydrostatic Pressure • (Low Pi) “Negative Pressure Pulmonary Edema”
Pulmonary Edema Caused by:
-reexpansion injury: may also damage capillaries
Pulmonary Edema Caused by: Oncotic
• Decreased Plasma Oncotic Pressure • (Low πc) • Caused by: overtransfusion leading to hypoalbuminemia
Pulmonary Edema: Pathogenesis
• Reduced Lymphatic Drainage • Normally handles ~ 20ml/hr
Reduce lymphatic drainage Caused by:
Obstruction, Tumor, Iatrogenic, Increased CVP • Interferes with drainage of thoracic duct
Pulmonary Edema Pathogenesis
Increased Capillary Permeability Decreased Interstitial Hydrostatic Pressure Decreased Plasma Oncotic Pressure Reduced Lymphatic Drainage
Pulmonary Edema : LVEDP
• Increased LV EDP – HF
Most common cause of pulmonary HTN
Pulmonary HTN • Increased Pulmonary Vascular Resistance • Most common cause
Three categories of pulmonary HTN Vasoconstrictive
Three categories: – • Ex. Hypoxia @ high altitude – Obstructive • Ex. thromboembolism – Obliterative • Ex. Destroyed capillary bed in emphysema
Three categories of pulmonary HTN:Obstructive
• Ex. thromboembolism
Three categories of pulmonary HTN: Obliterative
• Ex. Destroyed capillary bed in emphysema
CO (carbon monoxide) – Binds to Hb =
with 200x the affinity of O2
CO– Increases O2 affinity of remaining Hb
does not release O2 readily to the tissues – dissociation curve shifted to the Left
CO no change
– No change in PaO2
CO poisoning and O2 partial pressure
Oxygen partial pressure in the blood remains unchanged by CO poisoning (No cyanosis, no tachypnea)
CO is Dx by
measuring carboxyhemoglobin levels AND index of suspicion
Tx of CO
– Tx: 100% FiO2
Cigarette Smoking • Impaction
– Largest particles strike mucus surfaces, become trapped
Cigarette Smoking • Sedimentation
– Smoke particles settle in terminal & respiratory bronchioles, unlike gases, cannot diffuse to alvolar wall
Deposition of Particle Inhalation: Inhaled particles deposited in airways, mechanism based on
particle size
Impaction
large particles > 5 microns filtered by nasopharynx
Sedimentation
particles 1 to 5 microns deposit in terminal and respiratory bronchioles as laminar flow ceases
Diffusion –
particles < 0.1 micron, behave almost like gas. Most exhaled, but some deposits in alveoli, may be cleared by alveolar macrophages.
Clearance of Deposited Particles Two mechanisms:
• Particles deposited in conducting airways cleared by MCE (mucocilliary escalator) & swallowed
Particles deposited in gas exchange units cleared by
alveolar macrophages (“dust cells”)
Clearance of Deposited Particles inhibited By:
• Inhibited by: pollution, tobacco, steroids, radiation
MCE
• Seromucus glands & goblet cells secrete mucus 5-10 microns thick. (Gel top layer more viscous) IgA
Cilia sweeps mucus
~ 1mm/min in bronchioles; 2cm/min in trachea. Total clearance q 24 hrs.
ResFailure - Hypoxemia • “Normal” PaO2 calculation on
102 - 0.33 × age
RF Signs/Symptoms:
– ↓ PaO2 – Cyanosis – Tachycardia – Mental confusion
Tissue Hypoxia – vulnerability depends –
on tissue
Most vulnerable
CNS & Myocardium
Cessation of blood flow to cerebral cortex: • 4-6 sec
loss of function
Cessation of blood flow to cerebral cortex: 10-20 sec. =
l.o.c.
Cessation of blood flow to cerebral cortex 3-5 min. =
irreversible damage
Hypercapnia
• ⇑Work of breathing
Hypercapnia CNS receptor desensitization,
permissive hypercapnia
Hypercapnia renal compensation
( for ↑ H2CO3 - )
CNS desensitization from chronic hypercapnia →
dependency on hypoxic respiratory drive
Hypercapnia Treatment with O2 could suppress
hypoxic drive and increase CO2 retention/acidosis
Hypercapnia Answer is to give__________
low concentration (24-48% O2)
Hypercapnia, monitor this
monitor ABGs frequently to determine whether depression of ventilation is occurring.
The mucous film consists of a
superficial gel layer that traps inhaled particles and a deeper layer so it is propelled by cilia
